ArticleActa diabetologica2023
METTL14 promotes the development of diabetic kidney disease by regulating m
Article in Acta diabetologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- The lncRNA-m6A axis in cancer: a bidirectional regulatory network in tumor progression and therapeutic resistance.Journal of translational medicine · 2026Review
- Comprehensive Analysis of N6-Methyladenosine Modification Profiling in Diabetic Erectile Dysfunction.The world journal of men's health · 2026Article
- METTL14 knockdown mitigates HG-induced HK-2 cell apoptosis, inflammation, and ferroptosis by promoting SLC40A1.European journal of medical research · 2026Article
- N6-methyladenosine modification of CBLB affects LPS-induced endoplasmic reticulum stress in alveolar epithelial cells.Central-European journal of immunology · 2026Article
- Tubular injury in diabetic kidney disease: a focus on regulated cell death.Frontiers in endocrinology · 2026Review
- mFrontiers in cell and developmental biology · 2026Review
- The translational potential of m6A RNA methylation in DKD: emerging biomarkers for early detection and targeted therapies.Frontiers in medicine · 2026Review
- METTL3 alleviates renal tubular mitochondrial dysfunction by regulating the TUG1/PGC-1a axis in an IGF2BP2-dependent manner in diabetic nephropathy.Renal failure · 2025Article
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- lncRNA TUG1 and kidney diseases.BMC nephrology · 2025Review
- PIEZO1-Mediated Calcium Signaling and Podocyte Injury in Diabetic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025Article
- The role of N6-methyladenosine (mPeerJ · 2025Review
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- The latest progression of N6-methyladenosine (mFrontiers in endocrinology · 2025Review
- METTL14 derived from exosomes of M1 macrophages promotes high glucose-induced apoptosis, inflammation and oxidative stress in glomerular endothelial cells by mediating PAQR3 m6A modification.Clinical and experimental nephrology · 2024Article
- N6-methyladenosine (m6A) RNA modification in fibrosis and collagen-related diseases.Clinical epigenetics · 2024Review
- Diabetes and diabetic associative diseases: An overview of epigenetic regulations of TUG1.Saudi journal of biological sciences · 2024Review
- Autophagy, Pyroptosis and Ferroptosis are Rising Stars in the Pathogenesis of Diabetic Nephropathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- mInternational journal of biological sciences · 2024Article
- The mFrontiers in endocrinology · 2024Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundDiabetic kidney disease (DKD) is one of the most common diabetic complications. Endoplasmic reticulum stress (ERS) is an important step for renal tubular epithelial cell apoptosis during DKD progression. Herein, the role and regulatory mechanism of METTL14 in ERS during DKD progression were investigated.
methodsDKD animal and cell models were established by streptozotocin (STZ) and high glucose (HG), respectively. HE and Masson staining were performed to analyze renal lesions in DKD mouse. Cell viability and proliferation were determined by MTT and EdU staining, respectively. HK2 cell apoptosis was analyzed by flow cytometry. TUG1 m
resultsHG stimulation promoted apoptosis and increased ERS marker proteins (GRP78, CHOP and caspase12) expression in HK2 cells, while these changes were reversed by METTL14 knockdown. METTL14 inhibited TUG1 stability and expression level in an m
conclusionMETTL14 promoted renal tubular epithelial cell apoptosis and ERS by activating MAPK/ERK pathway through m
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.